Head Trauma Flashcards
who are at high risk of head injuries
young men and elderly previous head injuries residents of inner cities alcohol and drug abuse low income
what do over half of head injuries involve
alcohol
when do most deaths occur after head injury
within first hour
then peak at 7 hours- secondary effects
3rd peak later due to medical complications- high risk of pneumonia, DVT, PE
what are the components of the glasgow coma scale
eye opening (4-1)
- spontaneously
- to speech
- to pain
- none
verbal (5-1)
- orientated
- confused
- inappropriate
- incomprehensible
- no verbal
motor (6-1)
- obeying
- moves to localised pain
- flexion withdrawal from pain
- abnormal flexing (decorticate)
- abnormal extension (decerebrate)
- no motor response
which part of glasgow coma scale carries most significance
motor
what are the best and worst GCS scores
best 15
worst 3
when is a patient comatosed on GCS
8 or less
what are the parameters for head injury severity on GCS score
14/15, brief LOC= mild
9-13 = moderate
3-8= severe
patients with what risk factors should have a CT scan done within 1 hour of being identified
GCS< 13 on initial assessment GCS< 15 2 hours after injury suspected open/ depressed skull fracture any sign of basal skull fracture post traumatic seizure focal neurological deficit more than one episode of vomiting suspicion of NAI
who should get a CT if they experienced some LOC or amnesia since the injury
> 65
coagulopathy (medically induced or thrombophilia)
dangerous mechanism of injury
what does lacunar eyes mean
basilar skull fracture
what is battles sign
bruising over the mastoid - basilar skull fracture
what does any blood in CSF suggest
basilar skull #
what is DAI (found in CT in diffuse head injury)
diffuse axonal injury
what are the possible CT findings in a focal head injury
traumatic haemorrhage- extradural, subdural, intracerebral
contusion
what are the features of an extradural haematoma
blood cant cross suture lines - fills space
lens shape/ biconvex shape
more common in younger patients
what is the usual presentation of an extradural haematoma
injury with LOC has lucid interval in recovery rapid progression of neurological symptoms -deteriorating GCS -possible hemiparesis/ wekaness -unilateral fixed and dilated pupil -apnoea and death
what are the features of an acute subdural haematoma
more common in elderly
brain atrophy
bridging veins disrupted
will be hyPERdense
what will a chronic subdural haematoma look like on imaging
hyPOdense
what is an intracerebral haemoatoma
blood clot within the brain
what is coup and contra-coup
coup- brain hits side of head that is impacted
contra coup- brian hits opposite side
what causes a diffuse axonal injury
large shearing forces
what is the neurosurgical role in head injury
prevent secondary insults
- hypoxia
- hypotension
- mass lesions
- controlling ICP and CPP (cerebral perfusion pressure)
what formula calculated cerebral perfusion pressure
MAP - ICP
what maintains good cerebral perfusion pressure
maintained MAP (up) and ICP (down) at right levels
what are the basal cisterns
compartments within the subarachnoid space where the pia mater and arachnoid membrane are not in close approximation and cerebrospinal fluid (CSF) forms pools or cisterns
mass have vessels/ nerves running through them
what does closure of the basal cisterns do
increases ICP
how is ICP monitored
wire inserted into head
what is the medical management for raised ICP
sedation- propofol, benzodiazepines, barbiturates
maximise venous drainage of brain - head tilt of bed (30 degrees), cervical collars, ET tube ties
co2 control
osmotic diuretics - mannitol, hypertonic saline
CSF release- external ventricular drain
how does CO2 affect ICP
if CO2 is too high cerebral blood flow increases- increasing ICP
what happens if arterial CO2 drops too low
reduce blood flow to brain by too much
what is a decompressive craniectomy and when is it done
after all medical management of raised ICP is exhausted
take off part of cranium
saves lives but doesnt improve outcomes
why do BP changes have such a big impact in head injury
as lose autoregulation, will directly impact cerebral blood flow
why is nutrition important in head injury
need to feed patients NG early on
if not fed in 5-7 days after injury increase likelihood of death and mortality rate
why do axons swell up in DAI
as the injury (stretched, sheared, twisted or compressed) allows more ions and water into the axon
where do DAIs happen
where density difference is the greatest (grey/white interface)
what happens after DAI
excitotoxicity and apoptosis
inflammatory mediator (cytokines, interleukins) response
neuronal death
what is excitotoxicity
excitatory amino acids (gutamate) activates NMDA receptors
calcium mediated activation of proteases and lipases
cell death
do steroids help in head injuries
no- causes toxic swellings
what symptoms and signs suggest brainstem death
no pupil response no corneal reflex no gag reflex no vestibulo-ocular reflex (project cold water into one ear and look at eye movement) no motor response no respiration
what is the apnoea test
to look for brainstem death
Pre-oxygenate to look for a change in Co2 levels. Disconnect the ventilator and check pCO2 which must rise to 6 pKa
what are the possible long term complications of a head injury
Seizures Depression Alcohol and drug dependence Personality change Mood swings Aggression Recurrent behaviour – further head injuries Failure of relationships Loss of job suicide
what is ATLS
advanced trauma life support
- airway with C spine control
- breathing
- circulation
